Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome
The contribution of adipose tissue an autocrine and endocrine organ in the pathogenesis of infectious disease and metabolic syndrome is gaining attention. Adipose tissue and adipocytes are one of the major targets of T. cru...
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Main Authors: | , , , , , , |
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Format: | Article |
Language: | English |
Published: |
Wiley
2009-01-01
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Series: | Interdisciplinary Perspectives on Infectious Diseases |
Online Access: | http://dx.doi.org/10.1155/2009/824324 |
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Summary: | The contribution of adipose tissue an
autocrine and endocrine organ in the
pathogenesis of infectious disease and metabolic
syndrome is gaining attention. Adipose tissue
and adipocytes
are one of the major targets of T. cruzi infection. Parasites are detected 300 days postinfection in adipose tissue. Infection of adipose tissue and cultured adipocytes triggered local
expression of inflammatory mediators resulting in the upregulation of cytokine and chemokine
levels. Adipose tissue obtained from infected mice display an increased infiltration of
inflammatory cells. Adiponectin, an adipocyte specific protein, which exerts antiinflammatory
effects, is reduced during the acute phase of infection. The antiinflammatory regulator
peroxisome proliferator activated receptor-γ (PPAR-γ) is downregulated in infected cultured
adipocytes and adipose tissue. T. cruzi infection is associated with an upregulation of signaling
pathways such as MAPKs, Notch and cyclin D, and reduced caveolin-1 expression.
Adiponectin null mice have a cardiomyopathy and thus we speculate that the T. cruzi-induced
reduction in adiponectin contributes to the T. cruzi-induced cardiomyopathy. While T. cruzi infection causes hypoglycemia which correlates with mortality, hyperglycemia is associated
with increased parasitemia and mortality. The T. cruzi-induced increase in macrophages in
adipose tissue taken together with the reduction in adiponectin and the associated
cardiomyopathy is reminiscent of the metabolic syndrome. |
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ISSN: | 1687-708X 1687-7098 |